Chapter 7. Blood gases and acid-base balance Blood gases: oxygen (02) and carbon dioxide(C02) Oxygen transport To survive, a person must be able to absorb oxygen from the atmosphere and transport it to cells, where it is used in metabolism. Some

Blood. What element walks through your veins? How to determine a person's character by blood type. Astrological correspondence by blood type. There are four blood groups: I, II, III, IV. According to scientists, blood can determine not only the state of a person’s health and

Volume and physicochemical characteristics blood Volume of blood – total blood in the body of an adult is on average 6–8% of body weight, which corresponds to 5–6 liters. An increase in total blood volume is called hypervolemia, a decrease is called hypovolemia. Relative

Rheology is a field of mechanics that studies the characteristics of the flow and deformation of real continuous media, one of the representatives of which are non-Newtonian fluids with structural viscosity. A typical non-Newtonian fluid is blood. Blood rheology, or hemorheology, studies mechanical patterns and especially changes in the physical colloidal properties of blood during circulation at different speeds and at various areas vascular bed. The movement of blood in the body is determined by the contractility of the heart, functional state bloodstream, the properties of the blood itself. At relatively low linear flow velocities, blood particles move parallel to each other and the axis of the vessel. In this case, the blood flow has a layered character, and such a flow is called laminar.

If the linear speed increases and exceeds a certain value, different for each vessel, then the laminar flow turns into a disorderly, vortex flow, which is called “turbulent”. The speed of blood movement, at which laminar flow becomes turbulent, is determined using the Reynolds number, which for blood vessels is approximately 1160. Data on Reynolds numbers indicate that turbulence is possible only at the beginning of the aorta and in the areas of branching of large vessels. The movement of blood through most vessels is laminar. In addition to the linear and volumetric speed of blood flow, the movement of blood through the vessel is characterized by two more important parameters, the so-called “shear stress” and “shear rate”. Shear stress means the force acting on a unit surface of a vessel in a direction tangential to the surface and is measured in dynes/cm2, or Pascals. Shear rate is measured in reciprocal seconds (s-1) and means the magnitude of the velocity gradient between parallel moving layers of liquid per unit distance between them.

Blood viscosity is defined as the ratio of shear stress to shear rate, and is measured in mPas. The viscosity of whole blood depends on the shear rate in the range of 0.1 - 120 s-1. At a shear rate of >100 s-1, changes in viscosity are not so pronounced, and after reaching a shear rate of 200 s-1, blood viscosity remains virtually unchanged. The viscosity value measured at high speed shear (more than 120 - 200 s-1) is called asymptotic viscosity. The principal factors influencing blood viscosity are hematocrit, plasma properties, aggregation and deformability of cellular elements. Given the vast majority of red blood cells compared to white blood cells and platelets, the viscosity properties of blood are determined mainly by red cells.

The main factor determining blood viscosity is the volumetric concentration of red blood cells (their content and average volume), called hematocrit. The hematocrit, determined from a blood sample by centrifugation, is approximately 0.4 - 0.5 l/l. Plasma is a Newtonian fluid, its viscosity depends on temperature and is determined by the composition of blood proteins. Plasma viscosity is most affected by fibrinogen (plasma viscosity is 20% higher than serum viscosity) and globulins (especially Y-globulins). According to some researchers, more important factor What leads to a change in plasma viscosity is not the absolute amount of proteins, but their ratios: albumin/globulins, albumin/fibrinogen. The viscosity of blood increases during its aggregation, which determines the non-Newtonian behavior of whole blood; this property is due to the aggregation ability of erythrocytes. Physiological aggregation of erythrocytes is a reversible process. IN healthy body The dynamic process of “aggregation - disaggregation” continuously occurs, and disaggregation dominates over aggregation.

The ability of erythrocytes to form aggregates depends on hemodynamic, plasma, electrostatic, mechanical and other factors. Currently, there are several theories explaining the mechanism of erythrocyte aggregation. The most well-known theory today is the theory of the bridging mechanism, according to which bridges from fibrinogen or other large-molecular proteins, in particular Y-globulins, are adsorbed on the surface of the erythrocyte, which, with a decrease in shear forces, contribute to the aggregation of erythrocytes. The net aggregation force is the difference between the bridging force, the electrostatic repulsion force of negatively charged red blood cells, and the shear force causing disaggregation. The mechanism of fixation of negatively charged macromolecules on erythrocytes: fibrinogen, Y-globulins is not yet completely clear. There is a point of view that the adhesion of molecules occurs due to weak hydrogen bonds and van der Waals dispersion forces.

There is an explanation for the aggregation of erythrocytes through depletion - the absence of high molecular weight proteins near erythrocytes, resulting in the appearance of “interaction pressure”, similar in nature to osmotic pressure macromolecular solution, which leads to the convergence of suspended particles. In addition, there is a theory according to which erythrocyte aggregation is caused by erythrocyte factors themselves, which lead to a decrease in the zeta potential of erythrocytes and a change in their shape and metabolism. Thus, due to the relationship between the aggregation ability of erythrocytes and blood viscosity, it is necessary to assess the rheological properties of blood comprehensive analysis these indicators. One of the most accessible and widespread methods for measuring erythrocyte aggregation is the assessment of erythrocyte sedimentation rate. However, in its traditional version, this test is not very informative, since it does not take into account the rheological characteristics of blood.

1. Normalization of hemodynamics (restoration of blood flow speed in the periphery);

2. Controlled hemodilution (blood thinning and viscosity reduction);

3. Administration of disaggregants and anticoagulants (prevention of thrombus formation);

4. The use of drugs that reduce the rigidity of red blood cell membranes;

5. Normalization of the acid-base state of the blood;

6. Normalization of the protein composition of the blood (introduction of albumin solutions).

For the purpose of hemodilution and cell disaggregation, hemodez is used, as well as low-molecular dextrans, which increase the forces of electrostatic repulsion between formed elements due to an increase in the negative charge on their surface, reduce blood viscosity, attracting water into the vessels, cover the endothelium and vessels with a separating film, and form complex compounds with fibrinogen, reduce lipid concentrations.

Microcirculation disorders

In the organization of the circulatory system, we can distinguish the macrocirculation system - the heart pump, buffer vessels (arteries) and container vessels (veins) - and the microcirculation system. The task of the latter is to connect the circulatory system to the general circulation of the body and distribute cardiac output between organs according to their needs. Therefore, each organ has its own, unique microcirculation system, adequate to the function it performs. Nevertheless, it was possible to identify 3 main types of structure of the terminal vascular bed (classical, pavement and network) and describe their structure.

The microcirculation system, shown schematically in Fig. 4, consists of the following microvessels:

arterioles (diameter 100 µm or less);

precapillary arterioles or precapillaries or metarterioles (diameter 25 - 10 µm);

capillaries (diameter 2 – 20 µm);

postcapillary venules or postcapillaries (diameter 15 – 20 µm);

venules (diameter up to 100 µm).

In addition to these vessels, there are also arteriole-venular anastomoses - direct anastomoses between arterioles/arteries and venules/veins. Their diameter is from 30 to 500 microns, they are found in most organs.

Figure 4. Scheme of the microvasculature [according to Chambers, Zweifach, 1944].

The driving force of blood flow in the microcirculatory system is perfusion pressure or arteriovenous pressure difference. Therefore, this pressure is determined by the levels of total arterial and venous pressure, and its value can be influenced by cardiac function, total blood volume and total peripheral vascular resistance. The relationship between central and peripheral blood circulation is expressed by the formula Q =  P/ R, where Q is the intensity (volume velocity) of blood flow in the microcirculation system, P is the arteriovenous pressure difference, R is the peripheral (hydrodynamic) resistance in a given vascular bed. Changes in both P and R are leading in peripheral circulatory disorders. The lower the peripheral resistance, the greater the intensity of blood flow; the greater the value of peripheral resistance, the less the intensity of blood flow. Regulation of peripheral blood circulation and microcirculation in all organs is carried out by changing the resistance to current in their vascular system. An increase in blood viscosity increases hydrodynamic resistance and thus reduces the intensity of blood flow. The magnitude of hydrodynamic resistance depends much more on the radius of the vessels: hydrodynamic resistance is inversely proportional radius of blood vessels to the fourth power . It follows that changes in vascular lumen area (due to vasoconstriction or dilation) have a much greater effect on blood flow than factors such as viscosity or changes in pressure.

The main regulators of microcirculation are the adductor small arteries and arterioles and arteriovenous anastomoses. As a result of the expansion of the afferent arterioles, 1) the speed of blood flow increases, 2) the intracapillary pressure increases, and 3) the number of functioning capillaries increases. The latter will also be determined by the opening of the precapillary sphincters - the relaxation of two or more smooth muscle cells at the beginning of the capillaries.

Figure 5. Diagram of the main vessels of the microvasculature [according to Mchedlishvili, 1958].

A - smooth muscle cells of microvessels with vasomotor innervation; B - main capillary; B - capillaries forming a network. AVA - arterial-venous anastomosis.

The lumen of microvessels can actively change only if there are smooth muscle elements in their structure. In Fig. 5 the types of vessels that contain them are shaded. It follows that autonomic nerves innervate all blood vessels except capillaries. However, recent studies have shown the presence of areas of close relationships between terminal nerve elements and capillaries. They are specialized extensions of axons at the capillary wall, similar to extensions in the area of ​​axo-axonal synapses, i.e. form essentially “synapses along the way.” Probably this non-synaptic type of signal transmission, which ensures the free diffusion of neurotransmitters in the direction of microvessels, is the main way nervous regulation capillaries. In this case, regulation occurs not of one capillary, but of the entire vascular locus. When electrical stimulation of nerves (afferent and efferent) or under the influence of neurotransmitters, prostaglandins, histamine (including due to degranulation of mast cells), ATP, adrenaline and other vasoactive substances appear in the tissue. As a result, the state of endothelial cells mainly changes, transendothelial transport increases, endothelial permeability and tissue trophism change. Thus, the mediation of the regulatory-trophic influence of nerves on tissues through the circulatory system is carried out not only by roughly regulating the blood flow to the organ and its parts, but also by finely regulating the trophism itself through changing the state of the microvascular wall. On the other hand, the above materials show that innervation disorders relatively quickly lead to significant changes in the ultrastructure and permeability of capillaries. Consequently, microcirculatory disorders and, in particular, changes in vascular permeability should play an important role in the development of neurogenic dystrophies.

Changes in vascular tone or vascular sphincters can be caused by nervous, humoral and local regulatory mechanisms (Table 1).

Table 1.

Regulation of the microvascular bed

Note. The number of crosses indicates the degree of expression of regulation.

Nervous regulation carried out by the autonomic nervous system. Vasomotor nerves belong mainly to its sympathetic division(less often - parasympathetic) and abundantly innervate the arterioles of the skin, kidneys and celiac region. In the brain and skeletal muscles, these vessels are relatively weakly innervated. The mediator at synapses is norepinephrine, which always causes muscle contraction. The degree of contraction of vascular muscles depends directly on the frequency of impulses. Vascular tone at rest is maintained due to the constant flow of impulses through the vasomotor nerves at a frequency of 1-3 per second (so-called tonic impulses). At a pulse frequency of only about 10 per second, maximum vasoconstriction is observed. That., An increase in impulses in the vasomotor nerves leads to vasoconstriction, and a decrease leads to vasodilation., and the latter is limited by the basal tone of the vessels (i.e., the tone that is observed in the absence of impulses in the vasoconstrictor nerves or when they are cut).

Parasympathetic cholinergic vasodilator fibers innervate the vessels of the external genitalia, small arteries of the pia mater of the brain.

The nervous mechanism is also revealed by analyzing the dilation of skin vessels in response to mechanical or chemical irritation of the skin. This - axon reflex carried out using nociceptive (pain-conducting) nerve fibers and neuropeptides.

The sensitivity of muscle cells to vasoactive substances varies. Microvessels are 10-100 times more sensitive than large ones; the precapillary sphincters turned out to be the most sensitive in relation to the action of both constricting and dilating agents. Similar reactivity was found to occur with electrical stimulation (Table 2). Under pathological conditions, the sensitivity of microvessels to vasoactive substances changes.

table 2

Gradient of reactivity of the microcirculatory bed of the mesentery of rats

(after Zweifach,1961)

Microvascular reactivity also varies in different organs and tissues. This pattern is especially clear in relation to adrenaline (Table 3). Skin microvessels have the highest sensitivity to adrenaline.

Table 3

Reactivity of rat microvessels to nothreshold concentration

adrenaline (after Zweifach, 1961)

In recent years, the fact of the existence in the same neuron of two or more (up to seven) neurotransmitters of different chemical natures and in their different combinations has been proven. The widespread, if not ubiquitous, distribution of neuropeptides in autonomic nerves (for example, neuropeptide Y, vasoactive intestinal peptide, substance P, etc.) supplying blood vessels has been well proven by numerous immunohistochemical studies and indicates a significant increase in the complexity of the mechanisms of neural regulation of vascular tone. An even greater complication of these mechanisms is associated with the discovery of neuropeptides in the sensitive nerve fibers supplying blood vessels and their possible “effector” role in the regulation of vascular tone.

Humoral regulation carried out by hormones and chemicals released in the body. Vasopressin (antidiuretic hormone) and angiotensin II cause vasoconstriction. Callidin and bradykinin – vasodilation. Adrenaline secreted by the adrenal glands can have both a vasoconstrictor and a vasodilator effect. The response is determined by the number of - or -adrenergic receptors on the membrane of the vascular muscles. If α-receptors predominate in the vessels, then adrenaline causes them to constrict, and if the majority are β-receptors, then it causes expansion.

Local regulatory mechanisms provide metabolic autoregulation of peripheral circulation. They adapt local blood flow to the functional needs of the organ. In this case, metabolic vasodilatory effects dominate over the neural vasoconstrictor effects and, in some cases, completely suppress them. Microvessels dilate: lack of oxygen, metabolic products - carbon dioxide, an increase in H-ions, lactate, pyruvate, ADP, AMP and adenosine, many mediators of damage or inflammation - histamine, bradykinin, prostaglandins A and E and substance P. It is believed that dilation with The action of some mediators occurs due to the release of nitric oxide from endothelial cells, which directly relaxes smooth muscles. Damage mediators - serotonin, prostaglandins F, thromboxane and endothelins - constrict microvessels.

Regarding the ability of capillaries to actively narrow, the answer is rather negative, since there are no smooth muscle cells there. Those researchers who observe active narrowing of their lumen explain this narrowing by contraction of the endothelial cell in response to an irritant and protrusion of the cell nucleus into the capillary. Passive narrowing or even complete closure of the capillary occurs when the tension of their walls prevails over intravascular pressure. This condition occurs when blood flow through the afferent arteriole decreases. Significant expansion of capillaries is also difficult, since 95% of the elasticity of their walls comes from the surrounding connective substance. Only when it is destroyed, for example, by inflammatory exudate, increased intracapillary pressure can cause stretching of the capillary walls and their significant expansion.

In the arterial bed, pressure fluctuations are observed in accordance with the cardiac cycle. The amplitude of pressure fluctuation is called pulse pressure. In the terminal branches of the arteries and arterioles, the pressure drops sharply over several millimeters of the vascular network, reaching 30-35 mm Hg. at the end of the arterioles. This is due to the high hydrodynamic resistance of these vessels. At the same time, pulse pressure fluctuations significantly decrease or disappear and the pulsating blood flow is gradually replaced by a continuous one (with significant vasodilation, for example, during inflammation, pulse fluctuations are observed even in capillaries and small veins). However, rhythmic fluctuations in blood flow velocity can be noted in arterioles, metarterioles and precapillaries. The frequency and amplitude of these oscillations can be different, and they are not involved in adapting the blood flow to the needs of the tissues. It is assumed that this phenomenon - endogenous vasomotor - is due to the automaticity of contractions of smooth muscle fibers and does not depend on autonomic nervous influences.

It is possible that changes in blood flow in the capillaries also depend on leukocytes. Leukocytes, unlike erythrocytes, are not disc-shaped, but spherical in shape, and with a diameter of 6-8 microns, their volume exceeds the volume of erythrocytes by 2-3 times. When a leukocyte enters a capillary, it “gets stuck” at the mouth of the capillary for some time. According to researchers, it ranges from 0.05 seconds to several seconds. At this moment, the movement of blood in this capillary stops, and after the leukocyte slips into the microvessel, it is restored again.

The main forms of peripheral circulatory and microcirculation disorders are: 1. arterial hyperemia, 2. venous hyperemia, 3. ischemia, 4. stasis.

Thrombosis and embolism, which are not independent disorders of microcirculation, appear in this system and cause serious disturbances.

BIOPHYSICS OF THE CIRCULATORY SYSTEM

Hemodynamic indicators of blood flow are determined biophysical parameters of the entire cardiovascular system as a whole, namely its own characteristics of cardiac activity(For example stroke volume of blood), structural characteristics of blood vessels ( their radius and elasticity) and directly properties most blood (viscosity).

For description row processes, occurring as V separate parts circulatory system, and in it as a whole, methods of physical, analog and mathematical modeling are used. This chapter discusses blood flow patterns as fine, So and at some violations in cardiovascular system , which, in particular, include vasoconstriction (for example in education in them blood clots), change in blood viscosity.

Rheological properties of blood

Rheology(from Greek rheos - flow, flow, logos - teaching) - this is the science of deformation and fluidity of matter. Under blood rheology (hemorheology) we will understand study of the biophysical characteristics of blood as a viscous liquid.

Viscosity (internal friction) of the fluid- the property of a liquid to resist the movement of one part of it relative to another. The viscosity of a liquid is determined by Firstly, intermolecular interaction, limiting the mobility of molecules. The presence of viscosity leads to the dissipation of the energy of the external source causing the movement of the liquid and its transformation into heat. A fluid without viscosity (the so-called ideal fluid) is an abstraction. All real liquids have viscosity. An exception is the phenomenon of helium superfluidity at ultra-low temperatures (quantum effect)

Basic viscous flow law was established by I. Newton

(1687) - Newton's formula:

Where F[N] - internal friction force(viscosity) arising between layers of liquid when they shift relative to each other; [Pa s] dynamic viscosity coefficient liquid, characterizing the resistance of the liquid to displacement of its layers; - velocity gradient, showing how much the speed changesVwhen changing by unit distance in directionZwhen moving from layer to layer, otherwise - shear rate; S[m 2 ] - area of ​​contacting layers.

The internal friction force slows down the faster layers and accelerates the slower layers. Along with coefficient of dynamic viscosity are considering the so-called coefficient of kinematic viscosity (fluid density).

Liquids are divided into viscous properties into two types: Newtonian and non-Newtonian.

Newtonian called liquid , the viscosity coefficient of which depends only on its nature and temperature. For Newtonian fluids, the viscous force is directly proportional to the velocity gradient. Newton’s formula (1.a) is directly valid for them, the viscosity coefficient in which is a constant parameter independent of the fluid flow conditions.

A fluid is called non-Newtonian , the viscosity coefficient of which depends Not only by the nature of the substance and temperature, but also and on fluid flow conditions, in particular from the speed gradient. The viscosity coefficient in this case is not a constant of the substance. In this case, the viscosity of a liquid is characterized by a conditional viscosity coefficient, which relates to certain conditions of liquid flow (for example, pressure, speed). The dependence of the viscous force on the velocity gradient becomes nonlinear:

Where n characterizes the mechanical properties of a substance under given flow conditions. An example of non-Newtonian liquids are suspensions. If there is a liquid in which solid non-interacting particles are uniformly distributed, then such a medium can be considered homogeneous if we are interested in phenomena characterized by distances that are large compared to the size of the particles. The properties of such a medium primarily depend on the liquid. The system as a whole will have a different, higher viscosity, depending on the shape and concentration of particles. For case low particle concentrationsWITH the formula is correct:

WhereTO geometric factor - a coefficient depending on the geometry of particles (their shape, size) for spherical particles TOcalculated by the formula:

(2.a)

(R is the radius of the ball). For ellipsoidsTO increases and is determined by the values ​​of its semi-axes and their ratios. If the particle structure changes (for example, when flow conditions change), then the coefficient TOin (2), and therefore the viscosity of such a suspension will also change. Such a suspension is a non-Newtonian fluid. The increase in the viscosity of the entire system is due to the fact that the work of the external force during the flow of suspensions is spent not only on overcoming the true (Newtonian) viscosity caused by intermolecular interaction in the liquid, but also to overcome the interaction between it and structural elements.

Blood is a non-Newtonian fluid. This is largely due to the fact that she has internal structure , representing suspension of formed elements in solution - plasma. Plasma is practically a Newtonian fluid. Because the 93% formed elements make up red blood cells, That in simplified terms, blood is a suspension of red blood cells in saline solution . A characteristic property of erythrocytes is the tendency to form aggregates. If you apply a blood smear to a microscope stage, you can see how red blood cells “stick together” with each other, forming aggregates that are called coin columns. The conditions for the formation of aggregates are different in large and small vessels. This is primarily due to the ratio of the sizes of the vessel, aggregate and erythrocyte ( characteristic dimensions: )

There are three possible options here:

1. Large vessels (aorta, arteries):

D coc > d agr, d coc > d erythr

In this case, the gradient is small, red blood cells gather in aggregates in the form of coin columns. In this case, blood viscosity = 0.005 pa.s.

2. Small vessels (small arterines, arterioles):

In them, the gradient increases significantly and the aggregates break up into individual red blood cells, thereby reducing the viscosity of the system; for these vessels, the smaller the lumen diameter, the lower the blood viscosity. In vessels with a diameter of about 5 microns, the viscosity of blood is approximately 2/3 of the viscosity of blood in large vessels.

3. Microvessels (capillaries):

Observed reverse effect: with a decrease in the lumen of the vessel, the viscosity increases 10-100 times. In a living vessel, red blood cells are easily deformed and pass, without destruction, through capillaries even with a diameter of 3 microns. At the same time, they are greatly deformed, becoming like a dome. As a result, the surface of contact of erythrocytes with the capillary wall increases compared to an undeformed erythrocyte, promoting metabolic processes.

If we assume that in cases 1 and 2 the red blood cells are not deformed, then to qualitatively describe the change in the viscosity of the system, we can apply formula (2), which can take into account the difference in the geometric factor for a system of aggregates (K agr) and for a system of individual red blood cells K er : K agr K er, which determines the difference in blood viscosity in large and small vessels, then formula (2) is not applicable to describe processes in microvessels, since in this case the assumptions about the homogeneity of the medium and the hardness of the particles are not met.

Currently, the problem of microcirculation attracts much attention from theorists and clinicians. Unfortunately, the accumulated knowledge in this area has not yet received proper application in the practical activities of a doctor due to the lack of reliable and available methods diagnostics However, without understanding the basic laws of tissue circulation and metabolism, it is impossible to correctly use modern means infusion therapy.

The microcirculation system plays an extremely important role in providing tissues with blood. This occurs mainly due to the vasomotion reaction, which is carried out by vasodilators and vasoconstrictors in response to changes in tissue metabolism. The capillary network is 90% circulatory system, but 60-80% of it remains in an inactive state.

The microcirculatory system forms a closed blood flow between arteries and veins (Fig. 3). It consists of arterpoles (diameter 30-40 µm), which end in terminal arterioles (20-30 µm), which are divided into many metarterioles and precapillaries (20-30 µm). Further, at an angle close to 90°, rigid tubes devoid of a muscular membrane diverge, i.e. true capillaries (2-10 µm).

Rice. 3. A simplified diagram of the distribution of vessels in the microcirculatory system 1 - artery; 2 - terminal artery; 3 - arterrol; 4 - terminal arteriole; 5 - metarteril; 6 - precapillary with muscle sphincter (sphincter); 7 - capillary; 8 - collecting venule; 9 - venule; 10 - vein; 11 - main channel (central trunk); 12 - arteriolo-venular shunt.

Metarterioles at the precapillary level have muscle sphincter that regulates the flow of blood into the capillary bed and at the same time creates the peripheral resistance necessary for the functioning of the heart. Precapillaries are the main regulatory link of microcirculation, providing normal function macrocirculation and transcapillary exchange. The role of precapillaries as regulators of microcirculation is especially important in various disorders of volemia, when the level of bcc depends on the state of transcapillary exchange.

The continuation of the metarterioles forms the main canal (central trunk), which passes into the venous system. The collecting veins, which extend from the venous section of the capillaries, also flow here. They form prevenules, which have muscular elements and are capable of blocking the flow of blood from the capillaries. Prevenules collect into venules and form a vein.

There is a bridge between arterioles and venules - an arteriole-venous shunt, which is actively involved in the regulation of blood flow through microvessels.

Blood flow structure. Blood flow in the microcirculation system has a certain structure, which is determined primarily by the speed of blood movement. In the center of the blood flow, creating an axial line, there are red blood cells, which, together with the plasma, move one after another at a certain interval. This flow of red blood cells creates an axis around which other cells - white blood cells and platelets - are located. The erythrocyte current has the highest rate of advancement. Platelets and leukocytes located along the vessel wall move more slowly. Location components blood flow is quite definite and does not change at normal blood flow speed.

Directly in the true capillaries, the blood flow is different, since the diameter of the capillaries (2-10 microns) is less than the diameter of the red blood cells (7-8 microns). In these vessels, the entire lumen is occupied mainly by red blood cells, which acquire an elongated configuration in accordance with the lumen of the capillary. The wall layer of plasma is preserved. It is necessary as a lubricant for the gliding of red blood cells. Plasma also retains the electrical potential of the erythrocyte membrane and its biochemical properties, on which the elasticity of the membrane itself depends. In the capillary, the blood flow is laminar, its speed is very low - 0.01-0.04 cm/s at a blood pressure of 2-4 kPa (15-30 mm Hg).

Rheological properties of blood. Rheology - the science of fluidity liquid media. She studies mainly laminar flows, which depend on the relationship between inertial and viscosity forces.

Water has the lowest viscosity, allowing it to flow in any conditions, regardless of flow speed and temperature. Non-Newtonian fluids, which include blood, do not obey these laws. The viscosity of water is a constant value. Blood viscosity depends on a number of physicochemical parameters and varies widely.

Depending on the diameter of the vessel, the viscosity and fluidity of the blood change. The Reynolds number reflects feedback between the viscosity of the medium and its fluidity, taking into account the linear forces of inertia and the diameter of the vessel. Microvessels with a diameter of no more than 30-35 microns have positive influence on the viscosity of the blood flowing in them and its fluidity increases as it penetrates into narrower capillaries. This is especially pronounced in capillaries with a diameter of 7-8 microns. However, in smaller capillaries the viscosity increases.

Blood is in constant movement. This is its main characteristic, its function. As blood flow speed increases, blood viscosity decreases and, conversely, as blood flow slows down, it increases. However, there is also inverse relationship: The speed of blood flow is determined by viscosity. To understand this purely rheological effect, one must consider the blood viscosity index, which is the ratio of shear stress to shear rate.

The blood flow consists of layers of fluid that move in parallel, and each of them is under the influence of a force that determines the shear (“shear stress”) of one layer in relation to the other. This force is created by the systolic arterial pressure.

The viscosity of blood is influenced to a certain extent by the concentration of the ingredients it contains - red blood cells, nuclear cells, proteins, fatty acids, etc.

Red blood cells have an internal viscosity, which is determined by the viscosity of the hemoglobin they contain. The internal viscosity of an erythrocyte can vary within wide limits, which determines its ability to penetrate narrower capillaries and take on an elongated shape (thixitropia). Basically, these properties of the erythrocyte are determined by the content of phosphorus fractions in it, in particular ATP. Hemolysis of erythrocytes with the release of hemoglobin into plasma increases the viscosity of the latter by 3 times.

To characterize blood viscosity, proteins have exclusively important. A direct dependence of blood viscosity on the concentration of blood proteins has been revealed, especially A 1 -, A 2-, beta- and gamma-globulins, as well as fibrinogen. Albumin plays a rheologically active role.

Other factors that actively influence blood viscosity include fatty acid, carbon dioxide. Normal blood viscosity averages 4-5 cP (centipoise).

Blood viscosity, as a rule, is increased during shock (traumatic, hemorrhagic, burn, toxic, cardiogenic, etc.), dehydration, erythrocythemia and a number of other diseases. In all these conditions, microcirculation is primarily affected.

To determine viscosity, there are capillary-type viscometers (Oswald designs). However, they do not meet the requirement of determining the viscosity of moving blood. In this regard, viscometers are currently being designed and used, which are two cylinders of different diameters rotating on the same axis; blood circulates in the gap between them. The viscosity of such blood should reflect the viscosity of the blood circulating in the vessels of the patient’s body.

The most severe disturbance of the structure of capillary blood flow, fluidity and viscosity of blood occurs due to aggregation of erythrocytes, i.e. gluing red cells together to form “coin columns” [Chizhevsky A.L., 1959]. This process is not accompanied by hemolysis of red blood cells, as with agglutination of an immunobiological nature.

The mechanism of erythrocyte aggregation may be associated with plasma, erythrocyte or hemodynamic factors.

From the number plasma factors proteins play the main role, especially with high molecular weight, violating the ratio of albumin and globulins. A 1 - and a 2 - and beta-globulin fractions, as well as fibrinogen, have a high aggregation ability.

Violations of the properties of erythrocytes include changes in their volume, internal viscosity with loss of membrane elasticity and ability to penetrate the capillary bed, etc.

A slowdown in blood flow is often associated with a decrease in shear rate, i.e. occurs when blood pressure drops. Aggregation of erythrocytes is observed, as a rule, with all types of shock and intoxication, as well as with massive blood transfusions and inadequate artificial circulation [Rudaev Ya.A. et al., 1972; Soloviev G.M. et al., 1973; Gelin L. E., 1963, etc.].

Generalized aggregation of erythrocytes is manifested by the “sludge” phenomenon. The name for this phenomenon was proposed by M.N. Knisely, “sludging”, in English “swamp”, “mud”. Aggregates of erythrocytes undergo resorption in the reticuloendothelial system. This phenomenon always causes a difficult prognosis. It is necessary to promptly apply disaggregation therapy using low molecular weight solutions of dextran or albumin.

The development of “sludge” in patients can be accompanied by a very deceptive pinking (or redness) of the skin due to the accumulation of sequestered red blood cells in non-functioning subcutaneous capillaries. This clinical picture“sludge”, i.e. the last stage of development of erythrocyte aggregation and disruption of capillary blood flow is described by L.E. Gelin in 1963 under the name “red shock”. The patient’s condition is extremely serious and even hopeless if sufficiently intensive measures are not taken.